Vibrio cholerae: Difference between revisions

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Finally, ''Vibrio cholerae'' produces what is called a ZOT toxin, termed as "Zona Occludans Toxin". This toxin specifically attacks the zona occludans or "tight" junctions joining epithelial cells.
Finally, ''Vibrio cholerae'' produces what is called a ZOT toxin, termed as "Zona Occludans Toxin". This toxin specifically attacks the zona occludans or "tight" junctions joining epithelial cells.


==Treatment==
Water and electrolyte replacement are necessary in treating cholera. In some cases, [[tetracycline]] may be used. A vaccine is available outside the US, but it is short-lived and not currently recommended by the [[Centers for Disease Control and Prevention|CDC]].<ref name=CDC_Vacc>{{cite web | title=Is a vaccine available to prevent cholera? | work=CDC Disease Info: Cholera | url=http://www.cdc.gov/ncidod/dbmd/diseaseinfo/cholera_g.htm#Is%20a%20vaccine%20available%20to%20prevent%20cholera | accessdate=2007-01-21}}</ref> [[Fluoroquinolone]]s such as [[norfloxacin]] are used, but resistance has been reported.<ref>.Recently Hemendra Yadav reported his findings at A.I.I.M.S.,New Delhi that Ampicillin resistance has again decreased in V.cholerae strains of Delhi{{cite journal | author=Krishna BVS, Patil AB, Chandrasekhar MR | title=Fluoroquinolone-resistant ''Vibrio cholerae'' isolated during a cholera outbreak in India | jounal=Trans R Soc Trop Med Hyg | year=2006 | volume=100 | issue=3 | pages=224&ndash;26 | doi=10.1016/j.rstmh.2005.07.007 }}</ref>.


==Treatment==
===Antimicrobial regimen===
*1. '''WHO''' <ref>{{cite web | title = WHO. Cholera Outbreak: Assessing the Outbreak Response and Improving Preparedness.| url =http://www.who.int/cholera/publications/final%20outbreak%20booklet%20260105-OMS.pdf }}</ref> <ref>{{cite web | title = Prevention and control of cholera outbreaks: WHO policy and recommendations| url =http://www.who.int/cholera/prevention_control/recommendations/en/index4.html}}</ref>
::* Note: Antibiotic treatment for cholera patients with severe dehydration only
::* Adults
:::* Preferred regimen: [[Doxycycline]] 300 mg po single dose
:::* Alternative regimen: [[Tetracycline]] 12.5 mg/kg PO qid for 3 days
::* Pediatric
:::* Under 12 years old
::::* Preferred regimen: [[Erythromycin]] 12.5 mg/kg PO qid for 3 days
:::* Over 12 years old
::::* Preferred regimen: [[Doxycycline]] 300 mg po single dose
::::* Alternative regimen: [[Tetracycline]] 12.5 mg/kg PO qid for 3 days
*2. '''Pan American Health Organization''' <ref>{{cite web | title = PAHO. Recommendations for clinical management of cholera| url =file:///Users/censhanshan/Desktop/cholera_clin_management_ENG_rev_JUN%201.pdf }}</ref>
::* Note: Antibiotic treatment for cholera patients with moderate or severe dehydration
::*2.1 '''Adult'''
:::* Preferred regimen: [[Doxycycline]] 300 mg po single dose
:::* Alternative regimen (1): [[Ciprofloxacin]] 1 g PO single dose 
:::* Alternative regimen (2): [[Azithromycin]] 1 g PO single dose
::*2.2 '''Pediatric'''
:::*2.2.1 '''Children over 3 year, who can swallow tablets'''
::::* Preferred regimen (1): [[Erythromycin]] 12.5 mg/kg/ PO qid for 3 days
::::* Preferred regimen (2): [[Azithromycin]] 20 mg/kg PO in a single dose
::::* Alternative regimen (1): [[Ciprofloxacin]] suspension or tablets 20 mg/kg PO single dose
::::* Alternative regimen (2): [[Doxycycline]] suspension or tablets 2-4 mg/kg PO single dose
::::* Note: Although doxycycline has been associated with a low risk of yellowing of the teeth in children, its benefits outweigh its risks
:::*2.2.2 '''Children under 3 year, or infants who cannot swallow tablets'''
::::* Preferred regimen (1): [[Erythromycin]] suspension 12.5 mg/kg/ PO qid for 3 days
::::* Preferred regimen (2): [[Azithromycin]] suspension 20 mg/kg PO single dose
::::* Alternative regimen (1): [[Ciprofloxacin]] suspension 20 mg/kg PO single dose
::::* Alternative regimen (2): [[Doxycycline]] syrup 2-4 mg/kg PO single dose
::*2.3 '''Pregnancy'''
:::* Preferred regimen (!): [[Erythromycin]] 500 mg/ PO qid for 3 days 
:::* Preferred regimen (2): [[Azithromycin]] 1 g PO single dose


==References==
==References==
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[[nl:Vibrio cholerae]]
[[nl:Vibrio cholerae]]
[[ja:コレラ菌]]
[[ja:コレラ菌]]
[[sk:Vibrio cholerae]]
[[sk:Vibrio cholerae]
[[zh:霍亂弧菌]]
[[zh:霍亂弧菌]]


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Revision as of 18:14, 7 August 2015


Vibrio cholerae
TEM image
TEM image
Scientific classification
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Gamma Proteobacteria
Order: Vibrionales
Family: Vibrionaceae
Genus: Vibrio
Species: V. cholerae
Binomial name
Vibrio cholerae
Pacini 1854
This page is about microbiologic aspects of the organism(s).  For clinical aspects of the disease, see Cholera.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Vibrio cholerae is a gram negative bacterium with a curved-rod shape that causes cholera in humans.[1] V. cholerae and other species of the genus Vibrio belong to the gamma subdivision of the Proteobacteria.  There are two major strains of V. cholerae, classic and El Tor, and numerous other serogroups.

V. cholerae was first isolated as the cause of cholera by Italian anatomist Filippo Pacini in 1854, but his discovery was not widely known until Robert Koch, working independently thirty years later, publicized the knowledge and the means of fighting the disease.

Habitat

V. cholerae occurs naturally in the plankton of fresh, brackish, and salt water, attached primarily to copepods in the zooplankton. Coastal cholera outbreaks typically follow zooplankton blooms. This makes cholera a typical zoonosis.

Pathogenesis

V. cholerae colonizes the gastrointestinal tract, where it adheres to villous absorptive cells via pili, and secretes a binary toxin, called cholera toxin (CT). The two CT subunits are named A and B, and are synthesised in a 1:5 ratio. B subunits bind and internalize A subunits, which are processed to A1. The A1 form catalyses ADP ribosylation from NAD to the regulatory component of adenylate cyclase, thereby activating it. Increased adenylate cyclase activity increases cyclic AMP (cAMP) synthesis causing massive fluid and electrolyte efflux, resulting in diarrhea.

CT is encoded by the ctxAB genes on a specific filamentous bacteriophage. Transduction of this phage is dependent upon bacterial expression of the Toxin Coregulated Pilus (TCP), which is encoded by the V. cholerae pathogenicity island (VPI). VPI is generally only present in virulent strains and is laterally transferred. VPI was originally thought to encode a filamentous phage responsible for transfer. This theory was discredited by a study of 46 diverse V. cholerae isolates which found no evidence of VPI phage production. The generalized transduction phage CP-T1 has been shown to transduce the entire VPI which is then integrated at the same chromosomal location. Also, VPI has been shown to excise and circularize to produce pVPI via a specialised mechanism involving VPI-encoded recombinases. It is not known whether pVPI is involved in CP-T1 transduction or if it is perhaps a component of an alternative VPI mobilization mechanism.

Additionally, it produces two different proteases called chitinase and mucinase. Chitinase is responsible for the ability of Vibrio cholerae to enter copapods. Mucinase is a non-specific protease that assists entry into the human gastro-intestinal tract.

Finally, Vibrio cholerae produces what is called a ZOT toxin, termed as "Zona Occludans Toxin". This toxin specifically attacks the zona occludans or "tight" junctions joining epithelial cells.


References

  1. Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. ISBN 0838585299.

External links


bn:ভিব্রিও কলেরী de:Vibrio cholerae it:Vibrio cholerae he:Vibrio cholerae nl:Vibrio cholerae [[sk:Vibrio cholerae]


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